| Project/Area Number |
23592409
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nara Medical University |
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Principal Investigator |
FURUKAWA naoto 奈良県立医科大学, 医学部, 講師 (50347556)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Hiroshi 奈良県立医科大学, 医学部, 教授 (40178330)
YOSHIDA Shozo 奈良県立医科大学, 医学部, 助教 (40347555)
NARUSE Katsuhiko 奈良県立医科大学, 医学部, 助教 (70453165)
SHIGETOMI Hiroshi 奈良県立医科大学, 医学部, 助教 (20433336)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 卵巣癌 / 転写因子 / 細胞周期 / 酸化ストレス |
|---|
| Research Abstract |
We investigated the molecular targeted therapy in a viewpoint of Hepatocyte nuclear factor-1beta (HNF-1beta) in clear cell carcinoma of ovary. We found that G2 cell-cycle arrest is induced through adenoviral transfer of HNF-1beta. CHK1 kinase acts downstream of ATM/ATR kinase and plays an important role in the G2 checkpoint. G2 arrest of HNF-1beta (+) cells results from sustained CHK1 activation.Furthermore, HNF-1beta controls claspin expression, sustaining CHK1
protein phosphorylation.
These data indicated that the anticancer drug resistance of CCA may be caused by aberrant G2 arrest due to HNF-1A overexpression.
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